Short-term pioglitazone treatment prevents free fatty acid-induced hepatic insulin resistance in normal rats: Possible role of the resistin and adiponectin

2006 ◽  
Vol 339 (4) ◽  
pp. 1190-1196 ◽  
Author(s):  
Gangyi Yang ◽  
Ling Li ◽  
Yi Tang ◽  
Guenther Boden
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Hepatic Insulin Resistance ◽  
Short Term ◽  
Pioglitazone Treatment

scholarly journals Article Commentary: A Role for IR-β in the Free Fatty Acid Mediated Development of Hepatic Insulin Resistance?

2009 ◽  
Vol 2 ◽  
pp. BCI.S2996
Author(s):  
Samit Shah ◽  
Arthur G. Cox
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Pi3k Pathway ◽  
Hepatic Insulin Resistance ◽  
Hamster Model ◽  
High Concentrations ◽  
Nfκb Pathway

Several studies have been conducted to elucidate the role of free fatty acids (FFAs) in the pathogenesis of type 2 diabetes, but the exact molecular mechanism by which FFAs alter glucose metabolism in the liver is still not completely understood. 1 – 4 In a recent publication, Ragheb and coworkers have examined the effect of free fatty acid (FFA) treatment on insulin signaling and insulin resistance by using immunoprecipitation and immunoblotting to study the effect of high concentrations of insulin and FFAs on insulin receptor-beta (IR-β) and downstream elements in the PI3K pathway using the fructose-fed hamster model. 5 Their results clearly show that free fatty acids have an insignificant effect on IR-β and supports previous findings that FFAs lead to insulin resistance in the liver via the PKC-NFκB pathway. 2 , 3

scholarly journals Effects of free fatty acid elevation on hepatic insulin resistance and hepatic oxidative stress

2009 ◽  
Vol 17 (23) ◽  
pp. 2405
Author(s):  
Yan Lu ◽  
Ping Han ◽  
Sheng Zhao ◽  
Yong-Yan Zhang ◽  
Bing He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Hepatic Insulin Resistance ◽  
Hepatic Oxidative Stress

scholarly journals Effect of Weight Loss on Liver Free Fatty Acid Uptake and Hepatic Insulin Resistance

2009 ◽  
Vol 94 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Antti P. M. Viljanen ◽  
Patricia Iozzo ◽  
Ronald Borra ◽  
Mikko Kankaanpää ◽  
Anna Karmi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Uptake ◽  
Fat Content ◽  
Liver Fat ◽  
Hepatic Insulin Resistance ◽  
Acid Uptake ◽  
Liver Fat Content

Abstract Objective: Weight loss has been shown to decrease liver fat content and whole-body insulin resistance. The current study was conducted to investigate the simultaneous effects of rapid weight reduction with a very-low-calorie diet on liver glucose and fatty acid metabolism and liver adiposity. Hypothesis: We hypothesized that liver insulin resistance and free fatty acid uptake would decrease after weight loss and that they are associated with reduction of liver fat content. Design: Thirty-four healthy obese subjects (body mass index, 33.7 ± 8.0 kg/m2) were studied before and after a very-low-calorie diet for 6 wk. Hepatic glucose uptake and endogenous glucose production were measured with [18F]fluorodeoxyglucose during hyperinsulinemic euglycemia and fasting hepatic fatty acid uptake with [18F]fluoro-6-thia-heptadecanoic acid and positron emission tomography. Liver volume and fat content were measured using magnetic resonance imaging and spectroscopy. Results: Subjects lost weight (11.2 ± 2.9 kg; P < 0.0001). Liver volume decreased by 11% (P < 0.002), which was partly explained by decreased liver fat content (P < 0.0001). Liver free fatty acid uptake was 26% lower after weight loss (P < 0.003) and correlated with the decrement in liver fat content (r = 0.54; P < 0.03). Hepatic glucose uptake during insulin stimulation was unchanged, but the endogenous glucose production decreased by 40% (P < 0.04), and hepatic insulin resistance by 40% (P < 0.05). Conclusions: The liver responds to a 6-wk period of calorie restriction with a parallel reduction in lipid uptake and storage, accompanied by enhancement of hepatic insulin sensitivity and clearance.

Acute elevation of free fatty acid levels leads to hepatic insulin resistance in obese subjects

Metabolism ◽  
1987 ◽  
Vol 36 (5) ◽  
pp. 502-506 ◽  
Author(s):  
Stefano Bevilacqua ◽  
Riccardo Bonadonna ◽  
Giuseppe Buzzigoli ◽  
Claudio Boni ◽  
Demetrio Ciociaro ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Hepatic Insulin Resistance ◽  
Acute Elevation ◽  
Obese Subjects

scholarly journals Role of Insulin Resistance in MAFLD

2021 ◽  
Vol 22 (8) ◽  
pp. 4156
Author(s):  
Yoshitaka Sakurai ◽  
Naoto Kubota ◽  
Toshimasa Yamauchi ◽  
Takashi Kadowaki
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
De Novo Lipogenesis ◽  
Hepatic Insulin Resistance ◽  
Metabolic Dysfunction ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation

Many studies have reported that metabolic dysfunction is closely involved in the complex mechanism underlying the development of non-alcoholic fatty liver disease (NAFLD), which has prompted a movement to consider renaming NAFLD as metabolic dysfunction-associated fatty liver disease (MAFLD). Metabolic dysfunction in this context encompasses obesity, type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome, with insulin resistance as the common underlying pathophysiology. Imbalance between energy intake and expenditure results in insulin resistance in various tissues and alteration of the gut microbiota, resulting in fat accumulation in the liver. The role of genetics has also been revealed in hepatic fat accumulation and fibrosis. In the process of fat accumulation in the liver, intracellular damage as well as hepatic insulin resistance further potentiates inflammation, fibrosis, and carcinogenesis. Increased lipogenic substrate supply from other tissues, hepatic zonation of Irs1, and other factors, including ER stress, play crucial roles in increased hepatic de novo lipogenesis in MAFLD with hepatic insulin resistance. Herein, we provide an overview of the factors contributing to and the role of systemic and local insulin resistance in the development and progression of MAFLD.

scholarly journals Caloric Restriction Reverses Hepatic Insulin Resistance and Steatosis in Rats with Low Aerobic Capacity

Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5157-5164 ◽  
Author(s):  
Thomas A. Bowman ◽  
Sadeesh K. Ramakrishnan ◽  
Meenakshi Kaw ◽  
Sang Jun Lee ◽  
Payal R. Patel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Caloric Restriction ◽  
Visceral Obesity ◽  
Insulin Clearance ◽  
Hepatic Insulin Resistance ◽  
The Metabolic Syndrome ◽  
Cell Adhesion Molecule 1 ◽  
Muscle Triglyceride

Rats selectively bred for low aerobic running capacity exhibit the metabolic syndrome, including hyperinsulinemia, insulin resistance, visceral obesity, and dyslipidemia. They also exhibit features of nonalcoholic steatohepatitis, including chicken-wire fibrosis, inflammation, and oxidative stress. Hyperinsulinemia in these rats is associated with impaired hepatic insulin clearance. The current studies aimed to determine whether these metabolic abnormalities could be reversed by caloric restriction (CR). CR by 30% over a period of 2–3 months improved insulin clearance in parallel to inducing the protein content and activation of the carcinoembryonic antigen-related cell adhesion molecule 1, a main player in hepatic insulin extraction. It also reduced glucose and insulin intolerance and serum and tissue (liver and muscle) triglyceride levels. Additionally, CR reversed inflammation, oxidative stress, and fibrosis in liver. The data support a significant role of CR in the normalization of insulin and lipid metabolism in liver.

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